Journal articles: 'Fetal asphyxia'

1

Barton, D. P. J., M. J. Turner, and J. M. Stronge. "Intrapartum fetal asphyxia." American Journal of Obstetrics and Gynecology 162, no. 4 (April 1990): 1123. http://dx.doi.org/10.1016/0002-9378(90)91331-6.

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Galinsky, Robert, Vittoria Draghi, Guido Wassink, Joanne O. Davidson, Paul P. Drury, Christopher A. Lear, Alistair J. Gunn, and Laura Bennet. "Magnesium sulfate reduces EEG activity but is not neuroprotective after asphyxia in preterm fetal sheep." Journal of Cerebral Blood Flow & Metabolism 37, no. 4 (July 20, 2016): 1362–73. http://dx.doi.org/10.1177/0271678x16655548.

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Magnesium sulfate is now widely recommended for neuroprotection for preterm birth; however, this has been controversial because there is little evidence that magnesium sulfate is neuroprotective. Preterm fetal sheep (104 days gestation; term is 147 days) were randomly assigned to receive sham occlusion (n = 7), i.v. magnesium sulfate (n = 10) or saline (n = 8) starting 24 h before asphyxia until 24 h after asphyxia. Sheep were killed 72 h after asphyxia. Magnesium sulfate infusion reduced electroencephalograph power and fetal movements before asphyxia. Magnesium sulfate infusion did not affect electroencephalograph power during recovery, but was associated with marked reduction of the post-asphyxial seizure burden (mean ± SD: 34 ± 18 min vs. 107 ± 74 min, P < 0.05). Magnesium sulfate infusion did not affect subcortical neuronal loss. In the intragyral and periventricular white matter, magnesium sulfate was associated with reduced numbers of all (Olig−2+ve) oligodendrocytes in the intragyral (125 ± 23 vs. 163 ± 38 cells/field) and periventricular white matter (162 ± 39 vs. 209 ± 44 cells/field) compared to saline-treated controls ( P < 0.05), but no effect on microglial induction or astrogliosis. In conclusion, a clinically comparable dose of magnesium sulfate showed significant anticonvulsant effects after asphyxia in preterm fetal sheep, but did not reduce asphyxia-induced brain injury and exacerbated loss of oligodendrocytes.

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Clark, Richard B. "Definition of fetal asphyxia." American Journal of Obstetrics and Gynecology 163, no. 4 (October 1990): 1364. http://dx.doi.org/10.1016/0002-9378(90)90720-r.

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Richardson, Bryan S. "Fetal Adaptive Responses to Asphyxia." Clinics in Perinatology 16, no. 3 (September 1989): 595–611. http://dx.doi.org/10.1016/s0095-5108(18)30623-7.

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Low, J. A. "Fetal asphyxia and brain damage." Current Obstetrics & Gynaecology 3, no. 4 (December 1993): 213–18. http://dx.doi.org/10.1016/0957-5847(93)90041-m.

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Gruzdev, V. "Treatment of intrauterine fetal asphyxia." Kazan medical journal 20, no. 6 (August 11, 2021): 644. http://dx.doi.org/10.17816/kazmj76806.

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7

Espinoza, M., R. Riquelme, A. M. Germain, J. Tevah, J. T. Parer, and A. J. Llanos. "Role of endogenous opioids in the cardiovascular responses to asphyxia in fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 5 (May 1, 1989): R1063—R1068. http://dx.doi.org/10.1152/ajpregu.1989.256.5.r1063.

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Intravenous administration of the opioid receptor antagonist naloxone to asphyxiated fetal sheep increases the arterial blood pressure. We examined the hypothesis that endogenous opioids modify the cardiac output distribution during asphyxia due to changes in the vascular resistance of some fetal organs. Thirteen fetal sheep (0.8-0.9 of gestation) were chronically catheterized. Fetal asphyxia was induced by reducing the uterine blood flow with an inflatable occluder around the common internal iliac artery to approximately 50% of control for 40 min. Naloxone solution or the solvent alone was added for the last 20 min. Asphyxia caused hypertension, and the fetal arterial blood pressure further increased when asphyxiated fetuses received naloxone. Heart, brain, and adrenal blood flows increased due to the increase in blood pressure, with no changes in their vascular resistances. In contrast, kidney and carcass blood flows decreased, and their vascular resistances increased. We conclude that endogenous opioids inhibit the vasoconstriction of these vascular beds during fetal asphyxia.

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Lear, Christopher A., Joanne O. Davidson, Simerdeep K. Dhillon, Victoria J. King, Benjamin A. Lear, Shoichi Magawa, Yoshiki Maeda, Tomoaki Ikeda, Alistair J. Gunn, and Laura Bennet. "Effects of antenatal dexamethasone and hyperglycemia on cardiovascular adaptation to asphyxia in preterm fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 319, no. 6 (December 1, 2020): R653—R665. http://dx.doi.org/10.1152/ajpregu.00216.2020.

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Antenatal glucocorticoids improve outcomes among premature infants but are associated with hyperglycemia, which can exacerbate hypoxic-ischemic injury. It is still unclear how antenatal glucocorticoids or hyperglycemia modulate fetal cardiovascular adaptations to severe asphyxia. In this study, preterm fetal sheep received either saline or 12 mg im maternal dexamethasone, followed 4 h later by complete umbilical cord occlusion (UCO) for 25 min. An additional cohort of fetuses received titrated glucose infusions followed 4 h later by UCO to control for the possibility that hyperglycemia contributed to the cardiovascular effects of dexamethasone. Fetuses were studied for 7 days after UCO. Maternal dexamethasone was associated with fetal hyperglycemia ( P < 0.001), increased arterial pressure ( P < 0.001), and reduced femoral ( P < 0.005) and carotid ( P < 0.05) vascular conductance before UCO. UCO was associated with bradycardia, femoral vasoconstriction, and transient hypertension. For the first 5 min of UCO, fetal blood pressure in the dexamethasone-asphyxia group was greater than saline-asphyxia ( P < 0.001). However, the relative increase in arterial pressure was not different from saline-asphyxia. Fetal heart rate and femoral vascular conductance fell to similar nadirs in both saline and dexamethasone-asphyxia groups. Dexamethasone did not affect the progressive decline in femoral vascular tone or arterial pressure during continuing UCO. By contrast, there were no effects of glucose infusions on the response to UCO. In summary, maternal dexamethasone but not fetal hyperglycemia increased fetal arterial pressure before and for the first 5 min of prolonged UCO but did not augment the cardiovascular adaptations to acute asphyxia.

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Low, James A., Samuel K. Ludwin, and Stephanie Fisher. "Severe fetal asphyxia associated with neuropathology." American Journal of Obstetrics and Gynecology 175, no. 5 (November 1996): 1383–85. http://dx.doi.org/10.1016/s0002-9378(96)70063-7.

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Lear, Christopher A., Joanne O. Davidson, Georgia R. Mackay, Paul P. Drury, Robert Galinsky, Josine S. Quaedackers, Alistair J. Gunn, and Laura Bennet. "Antenatal dexamethasone before asphyxia promotes cystic neural injury in preterm fetal sheep by inducing hyperglycemia." Journal of Cerebral Blood Flow & Metabolism 38, no. 4 (April 7, 2017): 706–18. http://dx.doi.org/10.1177/0271678x17703124.

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Antenatal glucocorticoid therapy significantly improves the short-term systemic outcomes of prematurely born infants, but there is limited information available on their impact on neurodevelopmental outcomes in at-risk preterm babies exposed to perinatal asphyxia. Preterm fetal sheep (0.7 of gestation) were exposed to a maternal injection of 12 mg dexamethasone or saline followed 4 h later by asphyxia induced by 25 min of complete umbilical cord occlusion. In a subsequent study, fetuses received titrated glucose infusions followed 4 h later by asphyxia to examine the hypothesis that hyperglycemia mediated the effects of dexamethasone. Post-mortems were performed 7 days after asphyxia for cerebral histology. Maternal dexamethasone before asphyxia was associated with severe, cystic brain injury compared to diffuse injury after saline injection, with increased numbers of seizures, worse recovery of brain activity, and increased arterial glucose levels before, during, and after asphyxia. Glucose infusions before asphyxia replicated these adverse outcomes, with a strong correlation between greater increases in glucose before asphyxia and greater neural injury. These findings strongly suggest that dexamethasone exposure and hyperglycemia can transform diffuse injury into cystic brain injury after asphyxia in preterm fetal sheep.

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11

Hooper, S. B., M. J. Wallace, and R. Harding. "Amiloride blocks the inhibition of fetal lung liquid secretion caused by AVP but not by asphyxia." Journal of Applied Physiology 74, no. 1 (January 1, 1993): 111–15. http://dx.doi.org/10.1152/jappl.1993.74.1.111.

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We have examined whether the activation of Na+ channels, located on the luminal surface of pulmonary epithelial cells, mediates the inhibitory effects of both arginine vasopressin (AVP) and moderate asphyxia on fetal lung liquid secretion. Lung liquid secretion rates were measured in chronically catheterized fetal sheep during AVP infusions and during periods of asphyxia with and without an Na+ transport blocker (amiloride; 10(-4) M) present in lung liquid. Lung liquid secretion rates were also measured during epinephrine infusions with amiloride present in lung liquid. These secretion rates were compared with measurements made during a preceding control period. Both asphyxia and an infusion of AVP significantly reduced the rate of secretion of fetal lung liquid from 8.4 +/- 1.5 and 18.0 +/- 3.7 to 3.6 +/- 1.0 (P < 0.01) and 5.5 +/- 2.1 ml/h (P < 0.01), respectively. The addition of amiloride to lung liquid did not reverse the inhibitory effects of asphyxia on lung liquid secretion (8.6 +/- 0.8 vs. 0.7 +/- 0.4 ml/h) but did block the inhibitory effects of both epinephrine (14.8 +/- 4.4 vs. 13.8 +/- 3.1 ml/h) and AVP (18.0 +/- 3.7 vs. 19.5 +/- 5.0 ml/h). The addition of amiloride to lung liquid during fetal normoxia did not significantly affect fetal lung liquid secretion rates (8.2 +/- 1.1 vs. 7.4 +/- 0.7 ml/h). We conclude that the inhibitory effect of AVP on fetal lung liquid secretion, like that of epinephrine, involves the activation of luminal surface Na+ channels, whereas the inhibitory effect of asphyxia does not.

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12

Garnier, Yves, Richard Berger, Doris Pfeiffer, and Arne Jensen. "Low-dose flunarizine does not affect short-term fetal circulatory responses to acute asphyxia in sheep near term." Reproduction, Fertility and Development 10, no. 5 (1998): 405. http://dx.doi.org/10.1071/rd97081.

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Asphyxia is one of the major causes of perinatal brain damage and neuronal cell loss, which may result in psychomotor deficits during later development. It has been shown previously that the immature brain can be protected from ischemic injury by flunarizine, a class IV calcium antagonist. However, cardiovascular side-effects of flunarizine, when applied at the dosages used in those studies, have been reported. Recently, the present authors were able to demonstrate that even by injecting flunarizine at a far lower dosage (1 mg kg) estimated bodyweight) neuronal cell damage, caused by occlusion of both carotid arteries for 30 min, can be reduced in fetal sheep near term. The aim of the present study was, therefore, to examine whether low-dose flunarizine affects fetal cardiovascular responses to acute asphyxia in sheep near term. Ten fetal sheep were chronically instrumented at a mean gestational age of 132 1 days (term is at 147 days). Fetuses from the study group received a bolus injection of flunarizine (1 mg kg–1 estimated fetal weight) 60 min before asphyxia, whereas the solvent was administered to the fetuses from the control group. Organ blood flows, physiological variables and plasma concentrations of catecholamines were measured before, during and after a single occlusion of uterine blood flow for 2 min (i.e. at 0, 1, 2, 3, 4, and 30 min). Before asphyxia, the distribution of combined ventricular output and physiological variables, as well as concentrations of catecholamines, in fetuses from the control group were in the normal range for chronically prepared fetal sheep near term. During acute asphyxia there was a redistribution of cardiac output towards the central organs accompanied by a pronounced bradycardia and a rapid increase in arterial blood pressure. After asphyxia circulatory centralization did not resolve quite as rapidly as it developed, but was almost completely recovered at 30 min after the insult. There were nearly no differences in the time course of physiological and cardiovascular variables measured before, during and after acute intrauterine asphyxia between the control and study groups. From the present study it was concluded that low-dose flunarizine does not affect short-term fetal circulatory responses to acute asphyxia in sheep near term.

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13

Berry, D., A. Jobe, M. Ikegami, S. Seidner, A. Pettenazzo, and T. Elkady. "Pulmonary effects of acute prenatal asphyxia in ventilated premature lambs." Journal of Applied Physiology 65, no. 1 (July 1, 1988): 26–33. http://dx.doi.org/10.1152/jappl.1988.65.1.26.

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The effect of profound repetitive prenatal asphyxial insults on the cardiopulmonary function of premature ventilated lambs was studied. Twenty-nine fetal lambs (approximately 138 days gestational age) were exteriorized. In 16 of these lambs, the umbilical cord was occluded for 4 min then released for 10 min. This asphyxial episode was repeated until the arterial pH was approximately 7.00, and the mean arterial blood pressure was less than 40 mmHg and falling. The 13 control lambs were simply exteriorized with the umbilical circulation intact. The lambs were then ventilated for 3-4 h. There were no differences between the control vs. asphyxiated lambs in pulmonary compliances (0.57 and 0.58 ml.cmH2O-1.kg-1) wet-to-dry weight ratios (8.18 and 7.55), cardiac outputs (177.8 and 141.8 ml.kg-1.min-1), surfactant-saturated phosphatidylcholine pool sizes, or atrial and/or ductal shunts. Asphyxia did not interfere with the redirection of blood away from atelectatic lung segments created by bronchial obstruction with balloon catheters. Also, although the bidirectional flux of protein into and out of the airways of these preterm lambs was large relative to term lambs, there was no effect of asphyxia on this protein leak. In this animal model, prenatal asphyxia did not impact negatively on the severity of the respiratory failure.

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Shrivastava, Ayush, Jayant Vagha, and Rajendra Borkar. "Nucleated RBCs in umbilical cord blood as marker in cases of fetal asphyxia." International Journal of Contemporary Pediatrics 5, no. 1 (December 21, 2017): 203. http://dx.doi.org/10.18203/2349-3291.ijcp20175587.

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Background: World health organization (WHO) has defined perinatal asphyxia as a failure to initiate and sustain breathing at birth. HIE is one of the most common complication in an asphyxiated neonate because of its serious long term neuromotor sequalae among the survivors. Nucleated red blood cells (NRBC) count in umbilical cord of newborns is been suggested as a sign of birth asphyxia. As the present markers are not accurate in diagnosis and assessing the severity of fetal asphyxia, this study was undertaken to find the values of NRBCs in normal and asphyxiated neonates and the correlation of NRBCs with birth asphyxia.Methods: Eighty neonates with asphyxia along with eight healthy newborns were undertaken for two years study period. Maternal and neonatal information was recorded follow by clinical and laboratory evaluation. NRBC levels was determined per 100 white blood cells (WBC). After discharge, immediate follow-up of asphyxiated infants was performed. Neonates were divided into two groups, with favorable and unfavorable outcome based on discharge or death.Results: We observed that NRBC count with more than 10 per 100 WBC/mm3, had sensitivity of 88.75% and specificity of 100% in predicting complications of asphyxia, while in NRBC count with more than 10, the sensitivity and specificity were 88.75% and of 100%, respectively. Conclusions: We demonstrate that NRBC/100 WBC can be used as prognostic marker for neonatal asphyxia, which in combination with the severity of asphyxia could indicate high infant mortality, immediate outcome and complications of asphyxia

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15

Jensen, A., and MA Hanson. "Circulatory responses to acute asphyxia in intact and chemodenervated fetal sheep near term." Reproduction, Fertility and Development 7, no. 5 (1995): 1351. http://dx.doi.org/10.1071/rd9951351.

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The study concerned the role of the carotid sinus nerves in the effects of acute asphyxia on the fetal circulation. Fetal sheep (n = 12) were instrumented at approximately 130 days' gestation for placement of fetal vascular catheters and an occluder around the maternal descending aorta below the renal arteries. In 7 fetuses the carotid sinus nerves were cut. On the third post-operative day, asphyxia was produced by occluding the maternal aorta for 2 min and fetal blood flows were determined by the radio-labelled microsphere technique. In control, there were no differences between intact and denervated fetuses in blood gases, cardiovascular variables or blood flows, with the exception of lower blood flows to the cerebrum, caudate nucleus, kidney, skeletal muscle and scalp in the denervated group (P < 0.01). Fetal heart rate, cardiac output, stroke volume and the rate-pressure product were similar in asphyxia, with the exception that mean arterial pressure was lower in denervated fetuses after 2 min of asphyxia. Noradrenaline and adrenaline concentrations peaked at 2 min, then declined, the increase being smaller (P < 0.01) in denervated fetuses. Regional blood flows were similar in the two groups. Vascular resistance was lower in the placenta and abdominal aorta at 2 min in denervated fetuses. There were few differences in organ blood flows between intact and denervated fetuses, and the differences in flow in normoxia for the kidney, skeletal muscle and scalp (but not cerebrum, caudate nucleus and hippocampus) disappeared in asphyxia. This study confirms that section of the carotid sinus nerves has little effect on arterial blood pressure and fetal heart rate in normoxia but produces small differences in the responses to acute severe asphyxia, e.g. in arterial blood pressure and catecholamines, giving evidence for the operation of chemoreflexes. The lower blood flow to cerebrum, caudate nucleus, kidney, skeletal muscle and scalp in denervated fetuses in normoxia suggests a tonic vasodilatation, part of the drive for which comes from carotid chemo- or baroreceptors.

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Ganta, Suvarna Jyothi, and Sunanda R. Kulkarni. "Study of cord blood nucleated RBC’s as a marker for fetal asphyxia." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 6, no. 2 (January 31, 2017): 658. http://dx.doi.org/10.18203/2320-1770.ijrcog20170402.

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Background: Perinatal asphyxia is a serious problem globally and is a common cause of neonatal mortality and long term morbidity. Various Parameters are being used as predictors for birth asphyxia but the correlation between clinical presentation and the biochemical results has been unsatisfactory. NRBC count of the cord blood is reported in literature as a possible marker of perinatal asphyxia. In-utero hypoxic episode may induce a haemopoetic response of exaggerated erythropoiesis leading to the presence of nucleated RBC's in fetal circulation. The aim of this study was to investigate whether NRBC count of the cord blood can be a useful parameter to determine perinatal asphyxia.Methods: This prospective case control study was conducted in Chinmaya Mission hospital, Bangalore, India between July 2015 to June 2016.we have studied the NRBC counts from the cord blood of 50 neonates with perinatal asphyxia and 50 healthy neonates, thus comparing the results.Results: The mean NRBC /100 WBC for cases with birth asphyxia was 11.6 and that of the control group was 5.6. NRBC count was found to be significantly higher in neonates with low Apgar scores. There was correlation between the Apgar scores at 1st and at 5 minutes, the degree of Hypoxic Ischemic Encephalopathy and the NRBC counts.Conclusions: Therefore NRBC counts of the cord blood can be used as an effective tool to confirm perinatal asphyxia. It is a simple, quick, accurate and clinically effective test to diagnose and initiate treatment to prevent long term sequel of perinatal asphyxia.

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Tsikouras, Panagiotis, Anastasia Bothou, Zacharoula Koukouli, Bachar Manav, Constantinos Bouschanetzis, Dorelia Deuteraiou, Xanthi Anthoulaki, et al. "Physiopathological Mechanism and Assessment of Fetal Asphyxia." Open Journal of Obstetrics and Gynecology 07, no. 06 (2017): 617–22. http://dx.doi.org/10.4236/ojog.2017.76064.

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18

Low, James A. "Intrapartum fetal asphyxia: Definition, diagnosis, and classification." American Journal of Obstetrics and Gynecology 176, no. 5 (May 1997): 957–59. http://dx.doi.org/10.1016/s0002-9378(97)70385-5.

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Gavilanes, Danilo, Fabian Loidl, Wiel Honig, Arjan Blokland, Lara Spalldi, Erik Van Dijk, Harry Steinbusch, and Carlos Blanco. "Memory and Motor Behaviour after Fetal Asphyxia." Pediatric Research 44, no. 3 (September 1998): 449. http://dx.doi.org/10.1203/00006450-199809000-00216.

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Low, James A., H. Killen, and E. Jane Derrick. "Antepartum fetal asphyxia in the preterm pregnancy." American Journal of Obstetrics and Gynecology 188, no. 2 (February 2003): 461–65. http://dx.doi.org/10.1067/mob.2003.37.

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21

Andrew, M., H. O'Brodovich, and L. Mitchell. "Fetal lamb coagulation system during birth asphyxia." American Journal of Hematology 28, no. 3 (July 1988): 201–3. http://dx.doi.org/10.1002/ajh.2830280317.

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Wallace, MJ, SB Hooper, GJ McCrabb, and R. Harding. "Acidaemia enhances the inhibitory effect of hypoxia on fetal lung liquid secretion in sheep." Reproduction, Fertility and Development 8, no. 3 (1996): 327. http://dx.doi.org/10.1071/rd9960327.

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Previous studies have shown that moderate fetal asphyxia reduces the secretion rate of fetal lung liquid. The present aim was to determine the relative effects of the individual components of asphyxia (hypoxia, hypercapnia and acidaemia) on lung liquid secretion in fetal sheep. Fetal hyperoxia was also studied to determine the extent to which lung liquid secretion is restricted by the relatively low fetal blood PO2. As each manipulation of fetal blood gas tensions and pH treatment produced alterations in more than one aspect of blood composition, data from all treatment groups were combined and a multiple analysis of variance was performed to determine the separate effects of PaO2, PaCO2, SaO2 and pHa. Lung liquid secretion rate was significantly reduced when mean PaO2 values were below 24.5 mmHg (range 12.9-24.3 mmHg). When PaO2 values below 24.5 mmHg occurred in combination with pHa values below 7.275 (range 6.934-7.268) the secretion rates were further reduced. Alterations in pHa alone or in PaCO2 had no significant effect. These results indicate that hypoxia is the principal factor responsible for the inhibition of lung liquid secretion during asphyxia and that acidaemia enhances this inhibition.

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Lumbers, Eugenie R., Alistair J. Gunn, David Y. Zhang, June J. Wu, Linda Maxwell, and Laura Bennet. "Nonimmune hydrops fetalis and activation of the renin-angiotensin system after asphyxia in preterm fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 4 (April 1, 2001): R1045—R1051. http://dx.doi.org/10.1152/ajpregu.2001.280.4.r1045.

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This study examined the hypothesis that the development of hydrops fetalis after asphyxia in the 0.6 gestation sheep fetus would be associated with activation of the fetal renin-angiotensin system (RAS). Fetuses were randomly assigned to either sham occlusion ( n = 7) or to 30 min of asphyxia induced by complete umbilical cord occlusion for 30 min ( n = 8). Asphyxia led to severe bradycardia and hypotension that resolved after release of occlusion. After occlusion, plasma renin concentration was significantly increased in the asphyxia group compared with controls ( P < 0.005) after 3 min (16.3 ± 5.3 vs. 4.1 ± 1.3 ng · ml−1 · h−1), and 72 h (30.6 ± 6.3 vs. 3.7 ± 1.2 ng · ml−1 · h−1). Renal renin concentrations and mRNA levels were significantly greater in the asphyxia group after 72 h of recovery. All fetuses in the asphyxia group showed generalized tissue edema, ascites, and pleural effusions after 72 h of recovery. In conclusion, asphyxia in the preterm fetus caused sustained activation of the RAS, which was associated with hydrops fetalis.

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Löwensteyn, Yvette N., Natasha Housseine, Thokozani Masina, Joyce L. Browne, and Marcus J. Rijken. "Birth asphyxia following delayed recognition and response to abnormal labour progress and fetal distress in a 31-year-old multiparous Malawian woman." BMJ Case Reports 12, no. 9 (September 2019): e227973. http://dx.doi.org/10.1136/bcr-2018-227973.

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Reducing neonatal mortality is one of the targets of Sustainable Development Goal 3 on good health and well-being. The highest rates of neonatal death occur in sub-Saharan Africa. Birth asphyxia is one of the major preventable causes. Early detection and timely management of abnormal labour progress and fetal compromise are critical to reduce the global burden of birth asphyxia. Labour progress, maternal and fetal well-being are assessed using the WHO partograph and intermittent fetal heart rate monitoring. However, in low-resource settings adherence to labour guidelines and timely response to arising labour complications is generally poor. Reasons for this are multifactorial and include lack of resources and skilled health care staff. This case study in a Malawian hospital illustrates how delayed recognition of abnormal labour and prolonged decision-to-delivery interval contributed to birth asphyxia, as an example of many delivery rooms in low-income country settings.

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Singh, Nutan, Asheesh Kumar Gupta, and Ajay Kumar Arya. "A Study on Correlation of Umbilical Cord Arterial Blood pH with Perinatal Asphyxia & Early Neonatal Outcome." Asian Journal of Clinical Pediatrics and Neonatology 8, no. 2 (July 9, 2020): 30–35. http://dx.doi.org/10.47009/ajcpn.2020.8.2.6.

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Background: Perinatal asphyxia is one of the major causes of neonatal morbidity & mortality. Asphyxia can damage almost every organ of neonate. Our purpose was to determine the correlation of cord blood pH with birth asphyxia & early neonatal outcome. Subjects and Methods: A prospective study was conducted over a period of one year at STH Haldwani. We enrolled 108 term neonates with signs of fetal distress, thick MSL, non-reassuring NST & there were subjected for estimation of umbilical cord blood pH, APGAR score, outcome looked were resuscitation needed, NICU admission, delay in feed & encephalopathy (sarnat & sarnat stage). Results: In our study, cord blood pH had significant correlation with perinatal asphyxia(R=-0.926). Area under ROC curved showed that mean pH <7.1 (ROC=0.998) is very significant in predicting the adverse outcome. Conclusion: Cord blood pH is very sensitive and specific & has good correlation in predicting the birth asphyxia & adverse neonatal outcome. Measurement of cord blood pH is recommended in all the neonates with signs of fetal distress.

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., Sambedna, Amit Kumar, and Rita Chakore. "Outcomes and analysis of fetomaternal elements and delivery strategies with neonatal respiratory distress." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 10, no. 5 (April 23, 2021): 2001. http://dx.doi.org/10.18203/2320-1770.ijrcog20211527.

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Background: Perinatal asphyxia is one of the most important causes of morbidity and mortality in neonates. Perinatal asphyxia occurs in association with different maternal and fetal determinants. However, the relation of associated factors with perinatal asphyxia is not well studied. The aim of this study was to determine the association of maternofetal factors and mode of delivery with perinatal asphyxia in a tertiary care centre.Methods: This was a retrospective comparative study conducted in department of OBG in tertiary care health centre. A total 200 newborns were selected for study out of which100 newborns were with asphyxia at birth as study group and 100 non asphyxiated newborns were taken as control group. Maternal factor like age, parity, gestational age and fetal factor like weight at birth and mode of delivery were studied to established association on perinatal asphyxia.Results: Maternal factor like age, parity, gestational age had not significant relationship with perinatal asphyxia. Maximum number of babies delivered in both control and the study group were in the range of 2.6 to 3kg.In this study birth weight did not have significant relationship with perinatal asphyxia. Proportions of LSCS was comparatively higher in the study group though. The delivery mode did not have any statistically significant influence on the newborns affliction with birth asphyxia (p>0.05).Conclusions: Findings of this study highlight the need for the better obstetrical care and awareness of the possible presence of the risk factors of PNA (perinatal asphyxia) among mothers and fetus, so that the incidence and complications of PNA could be prevented or at least appropriately managed. It can reduce the high incidence of morbidity and mortality due to birth asphyxia.

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Cho, Kenta H. T., Mhoyra Fraser, Guido Wassink, Simerdeep J. Dhillon, Joanne O. Davidson, Justin M. Dean, Alistair J. Gunn, and Laura Bennet. "TLR7 agonist modulation of postasphyxial neurophysiological and cardiovascular adaptations in preterm fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 318, no. 2 (February 1, 2020): R369—R378. http://dx.doi.org/10.1152/ajpregu.00295.2019.

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Activation of Toll-like receptors (TLRs) after hypoxic-ischemic brain injury can exacerbate injury but also alleviate cell loss, as recently demonstrated with the TLR7 agonist Gardiquimod (GDQ). However, TLR agonists also modulate vascular function and neuronal excitability. Thus, we examined the effects of TLR7 activation with GDQ on cardiovascular function and seizures after asphyxia in preterm fetal sheep at 0.7 gestation (104 days, term ∼147 days). Fetuses received sham asphyxia or asphyxia induced by umbilical cord occlusion for 25 min or asphyxia followed by a continuous intracerebroventricular infusion of 3.34 mg of GDQ from 1 to 4 h after asphyxia. Fetuses were monitored continuously for 72 h postasphyxia. GDQ treatment was associated with sustained, moderate hypertension for 72 h ( P < 0.05), with a transient increase in heart rate. Electroencephalographic (EEG) power was suppressed for the entire postasphyxial period in both groups, whereas EEG spectral edge transiently increased during the GDQ infusion compared with asphyxia alone ( P < 0.05), with higher β- and lower δ-EEG frequencies ( P < 0.05). This increase in EEG frequency was not related to epileptiform activity. After the GDQ infusion, there was earlier onset of high-amplitude stereotypic evolving seizures, with increased numbers of seizures and seizure burden ( P < 0.05). Hemodynamic function and seizure activity are important indices of preterm wellbeing. These data highlight the importance of physiological monitoring during preclinical testing of potential neuroprotective strategies.

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Koehler, Raymond C., Zeng-Jin Yang, Jennifer K. Lee, and Lee J. Martin. "Perinatal hypoxic-ischemic brain injury in large animal models: Relevance to human neonatal encephalopathy." Journal of Cerebral Blood Flow & Metabolism 38, no. 12 (August 28, 2018): 2092–111. http://dx.doi.org/10.1177/0271678x18797328.

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Perinatal hypoxia-ischemia resulting in death or lifelong disabilities remains a major clinical disorder. Neonatal models of hypoxia-ischemia in rodents have enhanced our understanding of cellular mechanisms of neural injury in developing brain, but have limitations in simulating the range, accuracy, and physiology of clinical hypoxia-ischemia and the relevant systems neuropathology that contribute to the human brain injury pattern. Large animal models of perinatal hypoxia-ischemia, such as partial or complete asphyxia at the time of delivery of fetal monkeys, umbilical cord occlusion and cerebral hypoperfusion at different stages of gestation in fetal sheep, and severe hypoxia and hypoperfusion in newborn piglets, have largely overcome these limitations. In monkey, complete asphyxia produces preferential injury to cerebellum and primary sensory nuclei in brainstem and thalamus, whereas partial asphyxia produces preferential injury to somatosensory and motor cortex, basal ganglia, and thalamus. Mid-gestational fetal sheep provide a valuable model for studying vulnerability of progenitor oligodendrocytes. Hypoxia followed by asphyxia in newborn piglets replicates the systems injury seen in term newborns. Efficacy of post-insult hypothermia in animal models led to the success of clinical trials in term human neonates. Large animal models are now being used to explore adjunct therapy to augment hypothermic neuroprotection.

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Wassink, Guido, Robert Galinsky, Paul P. Drury, Eleanor R. Gunn, Laura Bennet, and Alistair J. Gunn. "Does Maturity Affect Cephalic Perfusion and T/QRS Ratio during Prolonged Umbilical Cord Occlusion in Fetal Sheep?" Obstetrics and Gynecology International 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/314159.

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T/QRS ratio monitoring is used to help identify fetal asphyxia. However, immature animals have greater capacity to maintain blood pressure during severe asphyxia, raising the possibility that they may show an attenuated T/QRS increase during asphyxia. Chronically instrumented fetal sheep at 0.6 of gestation (0.6 GA;n= 12), 0.7 GA (n= 12), and 0.8 GA (n= 8) underwent complete umbilical cord occlusion for 30 min, 25 min, or 15 min, respectively. Cord occlusion was associated with progressive metabolic acidosis and initial hypertension followed by severe hypotension, with a more rapid fall in mean arterial blood pressure (MAP) and carotid blood flow (CaBF) with advancing gestation. T/QRS ratio rose after occlusion more rapidly at 0.8 GA than in immature fetuses, to a similar final peak at all ages, followed by a progressive fall that was slower at 0.8 GA than in the immature fetuses. The increase in T/QRS ratio correlated with initial hypertension at 0.8 GA (P<0.05,R2= 0.38), and conversely, its fall correlated closely with falling MAP in all gestational groups (P<0.01,R2= 0.67). In conclusion, elevation of the T/QRS ratio is an index of onset of severe asphyxia in the last third of gestation, but not of fetal compromise.

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Booth, Lindsea C., Simon C. Malpas, Carolyn J. Barrett, Sarah-Jane Guild, Alistair J. Gunn, and Laura Bennet. "Renal sympathetic nerve activity during asphyxia in fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 1 (July 1, 2012): R30—R38. http://dx.doi.org/10.1152/ajpregu.00063.2012.

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The sympathetic nervous system (SNS) is an important mediator of fetal adaptation to life-threatening in utero challenges, such as asphyxia. Although the SNS is active well before term, SNS responses mature significantly over the last third of gestation, and its functional contribution to adaptation to asphyxia over this critical period of life remains unclear. Therefore, we examined the hypotheses that increased renal sympathetic nerve activity (RSNA) is the primary mediator of decreased renal vascular conductance (RVC) during complete umbilical cord occlusion in preterm fetal sheep (101 ± 1 days; term 147 days) and that near-term fetuses (119 ± 0 days) would have a more rapid initial vasomotor response, with a greater increase in RSNA. Causality of the relationship of RSNA and RVC was investigated using surgical (preterm) and chemical (near-term) denervation. All fetal sheep showed a significant increase in RSNA with occlusion, which was more sustained but not significantly greater near-term. The initial fall in RVC was more rapid in near-term than preterm fetal sheep and preceded the large increase in RSNA. These data suggest that although RSNA can increase as early as 0.7 gestation, it is not the primary determinant of RVC. This finding was supported by denervation studies. Interestingly, chemical denervation in near-term fetal sheep was associated with an initial fall in blood pressure, suggesting that by 0.8 gestation sympathetic innervation of nonrenal vascular beds is critical to maintain arterial blood pressure during the rapid initial adaptation to asphyxia.

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Low, James A. "Fetal Asphyxia: A Case Study of Translational Research." Journal of Obstetrics and Gynaecology Canada 35, no. 3 (March 2013): 258–62. http://dx.doi.org/10.1016/s1701-2163(15)30998-1.

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Gavilanes, Danilo, Fabian Loidl, Wiel Honig, Arjan Blokland, Lara Spalldi, Erik van Dijk, Harry Steinbusch, and Carlos Blanco. "Memory and Motor Behaviour after Fetal Asphyxia 1868." Pediatric Research 43 (April 1998): 318. http://dx.doi.org/10.1203/00006450-199804001-01891.

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Heinonen, Seppo, and Seppo Saarikoski. "Reproductive risk factors of fetal asphyxia at delivery." Journal of Clinical Epidemiology 54, no. 4 (April 2001): 407–10. http://dx.doi.org/10.1016/s0895-4356(00)00329-2.

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JENSEN, A., H. GIPS, M. HOHMANN, and W. KÜNZEL. "Fetal adrenal and circulatory responses to acute asphyxia." Acta Endocrinologica 117, no. 4_Suppl (April 1988): S227—S228. http://dx.doi.org/10.1530/acta.0.117s227-a.

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Oztekin, Deniz, Ipek Aydal, Ozgur Oztekin, Sabriye Okcu, Rengin Borekci, and Sivekar Tinar. "Predicting Fetal Asphyxia in Intrahepatic Cholestasis of Pregnancy." Obstetrical & Gynecological Survey 65, no. 3 (March 2010): 158–60. http://dx.doi.org/10.1097/01.ogx.0000369671.96283.30.

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Oztekin, Deniz, Ipek Aydal, Ozgur Oztekin, Sabriye Okcu, Rengin Borekci, and Sivekar Tinar. "Predicting fetal asphyxia in intrahepatic cholestasis of pregnancy." Archives of Gynecology and Obstetrics 280, no. 6 (March 26, 2009): 975–79. http://dx.doi.org/10.1007/s00404-009-1052-x.

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de Haan, Harmen H., Jos L. H. Van Reempts, Johan S. H. Vles, Jelte de Haan, and Tom H. M. Hasaart. "Effects of asphyxia on the fetal lamb brain." American Journal of Obstetrics and Gynecology 169, no. 6 (December 1993): 1493–501. http://dx.doi.org/10.1016/0002-9378(93)90424-h.

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Leijon, Ingemar. "The Prognostic Significance of Antenatal Diagnosis of Fetal Growth Retardation." International Journal of Technology Assessment in Health Care 8, S1 (January 1992): 176–81. http://dx.doi.org/10.1017/s0266462300013088.

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AbstractIntrauterine growth retardation is associated with high risk of perinatal asphyxia. The neonatal mortality rate of small-for-gestational-age (SGA) infants (birthweight ≤ 2 SD) in Sweden decreased from 5.6% in 1973 to 2.0% in 1987. During the same period, the number SGA infants with postnatal asphyxia (5 min Apgar score <7) decreased from 10% to 5%. Based on antenatal diagnosis of fetal growth retardation, an optimal time of delivery reduces the risk of major neurological and developmental sequelae of the individual infant.

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Wassink, Guido, Joanne O. Davidson, Simerdeep K. Dhillon, Mhoyra Fraser, Robert Galinsky, Laura Bennet, and Alistair J. Gunn. "Partial white and grey matter protection with prolonged infusion of recombinant human erythropoietin after asphyxia in preterm fetal sheep." Journal of Cerebral Blood Flow & Metabolism 37, no. 3 (July 20, 2016): 1080–94. http://dx.doi.org/10.1177/0271678x16650455.

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Perinatal asphyxia in preterm infants remains a significant contributor to abnormal long-term neurodevelopmental outcomes. Recombinant human erythropoietin has potent non-haematopoietic neuroprotective properties, but there is limited evidence for protection in the preterm brain. Preterm (0.7 gestation) fetal sheep received sham asphyxia (sham occlusion) or asphyxia induced by umbilical cord occlusion for 25 min, followed by an intravenous infusion of vehicle (occlusion-vehicle) or recombinant human erythropoietin (occlusion-Epo, 5000 international units by slow push, then 832.5 IU/h), starting 30 min after asphyxia and continued until 72 h. Recombinant human erythropoietin reduced neuronal loss and numbers of caspase-3-positive cells in the striatal caudate nucleus, CA3 and dentate gyrus of the hippocampus, and thalamic medial nucleus ( P < 0.05 vs. occlusion-vehicle). In the white matter tracts, recombinant human erythropoietin increased total, but not immature/mature oligodendrocytes ( P < 0.05 vs. occlusion-vehicle), with increased cell proliferation and reduced induction of activated caspase-3, microglia and astrocytes ( P < 0.05). Finally, occlusion-Epo reduced seizure burden, with more rapid recovery of electroencephalogram power, spectral edge frequency, and carotid blood flow. In summary, prolonged infusion of recombinant human erythropoietin after severe asphyxia in preterm fetal sheep was partially neuroprotective and improved electrophysiological and cerebrovascular recovery, in association with reduced apoptosis and inflammation.

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Quaedackers, J. S., V. Roelfsema, C. J. Hunter, E. Heineman, A. J. Gunn, and L. Bennet. "Polyuria and impaired renal blood flow after asphyxia in preterm fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 286, no. 3 (March 2004): R576—R583. http://dx.doi.org/10.1152/ajpregu.00592.2003.

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Renal impairment is common in preterm infants, often after exposure to hypoxia/asphyxia or other circulatory disturbances. We examined the hypothesis that this association is mediated by reduced renal blood flow (RBF), using a model of asphyxia induced by complete umbilical cord occlusion for 25 min ( n = 13) or sham occlusion ( n = 6) in chronically instrumented preterm fetal sheep (104 days, term is 147 days). During asphyxia there was a significant fall in RBF and urine output (UO). After asphyxia, RBF transiently recovered, followed within 30 min by a secondary period of hypoperfusion ( P < 0.05). This was mediated by increased renal vascular resistance (RVR, P < 0.05); arterial blood pressure was mildly increased in the first 24 h ( P < 0.05). RBF relatively normalized between 3 and 24 h, but hypoperfusion developed again from 24 to 60 h ( P < 0.05, analysis of covariance). UO significantly increased to a peak of 249% of baseline between 3 and 12 h ( P < 0.05), with increased fractional excretion of sodium, peak 10.5 ± 1.4 vs. 2.6 ± 0.6% ( P < 0.001). Creatinine clearance returned to normal after 2 h; there was a transient reduction at 48 h to 0.32 ± 0.02 ml·min-1·g-1(vs. 0.45 ± 0.04, P < 0.05) corresponding with the time of maximal depression of RBF. No renal injury was seen on histological examination at 72 h. In conclusion, severe asphyxia in the preterm fetus was associated with evolving renal tubular dysfunction, as shown by transient polyuria and natriuresis. Despite a prolonged increase in RVR, there was only a modest effect on glomerular function.

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Vlassaks, E., M. Nikiforou, E. Strackx, M. Hütten, O. Bekers, D. Gazzolo, G. Li Volti, P. Martinez-Martinez, B. W. Kramer, and A. W. D. Gavilanes. "Acute and chronic immunomodulatory changes in rat liver after fetal and perinatal asphyxia." Journal of Developmental Origins of Health and Disease 5, no. 2 (January 22, 2014): 98–108. http://dx.doi.org/10.1017/s2040174413000561.

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Hypoxic-ischemic encephalopathy (HIE) caused by fetal and perinatal asphyxia is an important cause of mortality in the neonatal period. Not only will asphyxia affect the brain but also other organs such as the liver and kidneys. Interestingly, it has been shown that liver damage is proportional to the severity of the asphyctic insult, implying an association between liver impairment and HIE. Accordingly, we investigated in an established rat model the acute and chronic hepatic response to both fetal (FA) and perinatal asphyxia (PA). In addition, we assessed whether fetal asphyctic preconditioning (PC) would have any beneficial effect on the liver. Inflammation, ceramide signaling and hepatocellular damage were analyzed in the livers of newborn and adult rats at several short- and long-term time points after both FA and PA. We found that although FA induced an acute inflammatory response, apoptotic mRNA levels and oxidative DNA damage were decreased at 96 h post FA. Whereas increased IL-6 and IL-10 mRNA levels were observed after PA, the combination of FA and PA (PC) attenuated the inflammatory response. Moreover, 6 h after PA anti-apoptotic genes were downregulated and associated with less lipid peroxidation, while preconditioned animals were comparable to controls. In summary, asphyctic PC seems to have an acute protective effect on the liver by modulating the inflammatory, apoptotic and anti-oxidative response. More insight into the hepatic response to asphyxia is necessary, as disturbed hepatic function is associated with metabolic diseases in later life.

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Hooper, S. B., and R. Harding. "Effect of beta-adrenergic blockade on lung liquid secretion during fetal asphyxia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 4 (October 1, 1989): R705—R710. http://dx.doi.org/10.1152/ajpregu.1989.257.4.r705.

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The hypothesis tested in this study was that beta-adrenergic stimulation is responsible for the inhibition of fetal lung liquid production during moderate fetal asphyxia. In chronically catheterized fetal sheep, net lung liquid production rates were measured over three consecutive periods: a control period, a period of reduced uterine blood flow (RUBF) or epinephrine infusion, and periods of RUBF or epinephrine infusion in the presence of the beta-adrenergic receptor antagonist propranolol. The net production rate of fetal lung liquid was decreased from a mean control value of 7.7 +/- 1.0 to 1.5 +/- 0.4 ml/h (P less than 0.001) by RUBF; the administration of propranolol had no further effect on these liquid production rates (1.1 +/- 0.5 ml/h). In other experiments epinephrine infusion reduced the net production rate of fetal lung liquid from a mean control value of 7.2 +/- 1.4 to 1.7 +/- 1.8 ml/h (P less than 0.025); the addition of propranolol reversed this inhibition (secretion rate 6.1 +/- 1.4 ml/h, P less than 0.005). We conclude that the inhibition of fetal lung liquid production induced by moderate fetal asphyxia does not solely result from catecholamine stimulation of pulmonary beta-receptors.

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Mogos, Magdalena, Catalin Gabriel Herghelegiu, Raluca Gabriela Ioan, Cringu Antoniu Ionescu, and Adrian Neacsu. "Determining an Umbilical Cord pH Cutoff Value for Predicting Neonatal Morbidity Related to Intrapartum Hypoxia." Revista de Chimie 70, no. 2 (March 15, 2019): 605–7. http://dx.doi.org/10.37358/rc.19.2.6965.

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Intrapartum hypoxia can lead to perinatal asphyxia, acidosis, neuronal injury, long-term morbidity or even death. Intrapartum asphyxia and hypoxia can be predicated by fetal acidosis. Umbilical cord gases are used to evaluate a newborn�s acid-base status and the presence of hypoxia. Depending on what references are used, normal values for umbilical cord gases can wildly vary. Although most papers set a pH threshold of [7.2 for fetal acidosis / acidemia, some studies suggest that neonatal morbidity and mortality is increased only when the pH threshold is set below / cut-off value is 7.0. We did a retrospective study and evaluated all newborns from singleton term births in INSMC Alessandrescu Rusescu between 2010 - 2012. We found 83 cases of intrapartum asphyxia (IA) and 25 cases of hypoxic ischemic encephalopathy (HIE). Also a control group of 100 normal term newborns were randomly selected. The IA and HIE showed significant lower mean umbilical cord pH values compared to the control group (7.19, respectively 7.12 compared to 7.28). Using the Youden index we calculated pH a cutoff value of 7.25 for the prediction of IA and of 7.16 for the prediction of HIE. While a low Apgar score can be a predictor of neonatal outcome and may be determined by fetal hypoxia, it remains a subjective evaluation with variable intra-observer reliability. Thus it is important to have an objective test able to accurately diagnose perinatal asphyxia and predict the neonatal outcome.

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Wang, Qiuping, Weihua Yang, Lie Li, Guokai Yan, Huihui Wang, and Jianqiang Li. "Late pregnancy analysis with Yunban’s remote fetal monitoring system." International Journal of Distributed Sensor Networks 15, no. 3 (March 2019): 155014771983283. http://dx.doi.org/10.1177/1550147719832835.

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With the adoption of the two-child policy, there has been a large increase in women of older maternal and high-risk pregnant women. So, it is necessary to analyze the health status of women in the late pregnancy on time. To analyze the effect on using remote fetal monitoring on women in the late pregnancy, we selected women in the late stage of pregnancy in our hospital as research subjects. They were randomly divided into two groups: the experimental group, which engaged in remote fetal monitoring, and the control group, which adopted traditional cardiac monitoring. In order to get more effective data, we used the Kalman filter and audio repair algorithms to preprocess the collected data. During follow-up observation, we compared the two groups using neonatal cardiac monitoring by employing the non-stress test and observed the occurrence of neonatal asphyxia. The incidence of neonatal abnormal non-stress test in the experimental group and the control group was 33.6% and 17.3%, respectively; the difference was statistically significant ( p < 0.05). The incidence of neonatal asphyxia in the experimental group was 12.5%, which was significantly lower than in the control group (30%; p < 0.05). We have found that women in the late stage of pregnancy who adopted remote fetal monitoring could detect abnormal non-stress test earlier and thus increase in the detection of rate of neonatal asphyxia.

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Alebachew Bayih, Wubet, Tadesse Gashaw Tezera, Abebaw Yeshambel Alemu, Demeke Mesfin Belay, Habtamu Shimelis Hailemeskel, and Metadel Yibeltal Ayalew. "Prevalence and determinants of asphyxia neonatorum among live births at Debre Tabor General Hospital, North Central Ethiopia: a cross-sectional study." African Health Sciences 21, no. 1 (April 16, 2021): 385–96. http://dx.doi.org/10.4314/ahs.v21i1.49.

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Background: More than one third of the neonatal deaths at Neonatal Intensive Care Unit of Debre Tabor General Hos- pital (DTGH) are attributable to birth asphyxia. Most of these neonates are referred from maternity ward of the hospital. However, there is no recent evidence on the prevalence and specific determinants of birth asphyxia at DTGH. Besides, public health importance of factors like birth spacing weren’t addressed in the prior studies. Methods: A cross sectional study was conducted on a sample of 240 newborns at delivery ward. The collected data were cleaned, coded and entered into Epi -data version 4.2 and exported to Stata version 14. Binary logistic regression model was considered and statistical significance was declared at P< 0.05 using adjusted odds ratio. Results: The prevalence of asphyxia neonatorum was 6.7 % based on the fifth minute APGAR score. From multi-variable logistic regression analysis, antenatal obstetric complications (AOR = 2.63, 95% CI: 3.75, 14.29), fetal malpresentation (AOR = 3.17, 95% CI: 1.21, 15.20), premature rupture of fetal membranes (AOR = 6.56, 95% CI: 3.48, 18.12) and meconium stained amniotic fluid (AOR = 2.73, 95% CI: 1.76, 14.59) were significant predictors. Conclusion: The prevalence of fifth minute asphyxia neonatorum was relatively low. Fortunately, its predictors are modifi- able. Thus, we can mitigate the problem even with our limited resources such as enhancing the existing efforts of antenatal and intra-partum care, which could help early detection and management of any obstetric and neonatal health abnormality.” Keywords: Birth asphyxia; asphyxia neonatorum; prevalence; determinants; Ethiopia.

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Lestari, Siti, Dyah Dwi Astuti, and Fachriza Malika Ramadhani. "Analisis Faktor Fetus dan Tali Pusat terhadap Risiko Asphyxia Perinatal di Surakarta." Jurnal Ilmu Keperawatan Anak 3, no. 1 (May 31, 2020): 16. http://dx.doi.org/10.32584/jika.v3i1.521.

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Asfiksia perinatal merujuk pada kekurangan oksigen selama persalinan, sehingga berpotensi menyebabkan kematian dan kecacatan. WHO memperkirakan 4 juta anak terlahir dengan asfiksia setiap tahun, dimana 1 juta di antaranya meninggal dan 1 juta anak bertahan hidup dengan gejala sisa neurologis yang parah. Penelitian ini bertujuan untuk menganalisis faktor risiko fetal dan tali pusat pada asfiksia neonatal.Penelitian dilakukan di lakukan di RS Dr Moewardi Surakarta dengan pendekatan quantitative retrospective case control study. Data diambil dari rekam medis antara tahun 2013-2018. Penelitan ini melibatkan 264 neonatal yang terdiri dari 88 kelompok kasus dan 176 kelompok control. Kelompok kasus adalah bayi dengan diagnosa asfiksia yang dilakukan analisis terhadap faktor risiko fetal, sedangkan bayi yang tidak mengalami asfiksia dijadikan kelompok kontrol. Hasil analisis statistik uji Chi-Square dan Fisher Exact ditemukan bahwa kelahiran prematur (OR 2,07 CI 95% P 0,02), persalinan dengan tindakan (OR 3,61 CI 95% P 0,00), berat bayi (OR 2,85 CI 95% P 0,00), posisi janin (OR 2,37 CI 95% P 0,05), tali pusat ( QR 3,071 CI 95% P 0,01) berisiko terhadap insiden asfiksia perinatal. Air ketuban yang bercampur meconium (OR 1,51 CI 95% P 0,16) tidak memiliki risiko dengan Asfiksia perinatal. Kesimpulan: Risiko terhadap insiden asfiksia perinatal meliputi kelahiran prematur, persalinan dengan tindakan, berat bayi, posisi janin, dan tali pusat.Perinatal asphyxia refers to a lack of oxygen during labor, which has the potential to cause death and disability. WHO estimates 4 million children born with asphyxia each year, in which 1 million dies and 1 million survive with severe neurological sequelae. This study aims to analyze fetal and umbilical risk factors in neonatal asphyxia.This research is a quantitative retrospective case-control study, which was conducted at The Dr. Moewardi hospital, Surakarta. Data was taken from medical records from 2013-2018. The case group was patients diagnosed asphyxia, while those who did not experience asphyxia were treated as a control group. A total of 264 samples, consisting of 88 case group respondents and 176 control group respondents. Statistical analysis Chi- Square and Fisher Exact found that preterm birth (OR 2.07 CI 95% P 0.02), labor with instrument or complication (OR 3.61 CI 95% P 0.00), infant weight (OR 2.85 CI 95% P 0, 00), fetal position (OR 2.37 CI 95% P 0.05), umbilical cord (QR 3.071 CI 95% P 0.01) are at risk for the incidence of perinatal Asphyxia. The amniotic fluid mixed with meconium (OR 1.51 CI 95% P 0.16) has no risk with perinatal asphyxia.The risk factors of incidences of perinatal asphyxia were preterm birth, labor with instrument or complication, baby weight, fetal position and umbilical cord.

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Low, J. "Predictive value of electronic fetal monitoring for intrapartum fetal asphyxia with metabolic acidosis." Obstetrics & Gynecology 93, no. 2 (February 1999): 285–91. http://dx.doi.org/10.1016/s0029-7844(98)00441-4.

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Bennet, Laura, Lindsea C. Booth, Noha Ahmed-Nasef, Justin M. Dean, Joanne Davidson, Josine S. Quaedackers, and Alistair J. Gunn. "Male disadvantage? Fetal sex and cardiovascular responses to asphyxia in preterm fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 3 (September 2007): R1280—R1286. http://dx.doi.org/10.1152/ajpregu.00342.2007.

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Clinically and experimentally male fetuses are at significantly greater risk of dying or suffering injury at birth, particularly after premature delivery. We undertook a retrospective cohort analysis of 60 female and 65 male singleton preterm fetal sheep (103–104 days, 0.7 gestation) with mean arterial blood pressure (MAP), heart rate, and carotid and femoral blood flow recordings during 25 min of umbilical cord occlusion in utero. Occlusions were stopped early if fetal MAP fell below 8 mmHg or if there was asystole for >20 s. Fetuses that were able to complete the full 25-min period of occlusion showed no differences between sexes for any cardiovascular responses. Similar numbers of occlusions were stopped early in males (mean: 21 min, n = 16) and females (mean: 23 min, n = 16); however, they showed different responses. Short-occlusion males ( n = 16) showed a slower initial fall in femoral vascular conductance, followed by greater bradycardia, hypotension, and associated organ hypoperfusion compared with full-occlusion fetuses. In contrast, short-occlusion females ( n = 16) showed a significantly more rapid early increase in femoral vascular conductance than the full-occlusion fetuses, followed by worsening of bradycardia and hypotension that was intermediate to the full-occlusion fetuses and short-occlusion males. Among all fetuses, MAP at 15 min of occlusion, corresponding with the time of the maximal rate of fall, was correlated with postmortem weight in males ( R2 = 0.07) but not females. In conclusion, male and female fetuses showed remarkably similar chemoreflex and hemodynamic responses to severe asphyxia, but some males did show impaired hemodynamic adaptation within the normal weight range.

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LOW, JAMES A., RAHI VICTORY, and E. JANE DERRICK. "Predictive Value of Electronic Fetal Monitoring for Intrapartum Fetal Asphyxia With Metabolic Acidosis." Obstetrics & Gynecology 93, no. 2 (February 1999): 285–91. http://dx.doi.org/10.1097/00006250-199902000-00024.

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Field, David R., Julian T. Parer, Ron Auslender, B. Wycke Baker, Brian K. Ross, and Craig H. Leicht. "Fetal heart rate variability and cerebral oxygen consumption in fetal sheep during asphyxia." European Journal of Obstetrics & Gynecology and Reproductive Biology 42, no. 2 (November 1991): 145–53. http://dx.doi.org/10.1016/0028-2243(91)90175-k.

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Journal articles on the topic 'Fetal asphyxia'

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